Facilitators and Barriers of Medication Adherence Based on Beliefs of Persons with Bipolar Disorder: A Qualitative Study.

One of the big challenges in treating individuals with bipolar disorder (BD) is nonadherence to medication. This is the principal factor associated with a worse prognosis or outcome of the disease. This study aimed to explore and analyze the individual perceptions that people with BD have about the positive and negative aspects when taking medication. A descriptive and interpretative study was carried out using the qualitative research paradigm with the use of the analytical technique of discourse analysis, extracting the data through the completion of focus groups. Participants' speech was digitally audio-recorded in digital format. In order to complete the codification of the participants' speech content, we relied on the qualitative data analysis (using the QRS NVivo 10 computer software). Thirty-six participants diagnosed with bipolar disorder took part in our study. In the participants' speech concerning the main barriers to pharmacological treatment, three key topics were identified. Perceived facilitators were summarized in four factors. The main facilitators regarding the use of pharmacological treatment in individuals with BD were the ones related with the perceived need for treatment in the acute phase, the recognition of the illness, the shared clinical decision, and the causal biological attribution in the chronic phase. In terms of perceived barriers, social control was identified in both phases, adverse effects in the acute phase, and the absence of effective treatment in the chronic state.

Antidepressants induce autophagy dependent-NLRP3-inflammasome inhibition in Major depressive disorder.

Major Depressive Disorder (MDD, ICD-10: F-33) is a prevalent illness in which the pathogenic mechanism remains elusive. Recently an important role has been attributed to neuro-inflammation, and specifically the NLRP3-inflammasome complex, in the pathogenesis of MDD. This suggests a key role for immunomodulation as a key pathway in the treatment of this disorder. This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients. Antidepressant treatment induced inflammasome inhibition was observed by decreased serum levels of IL-1ß and IL-18 and decrease of NLRP3 and IL-1ß (p17) protein expression. This was also observed under stress-induced depressive behaviour and inflammasome activation in C57Bl/6 mice in vivo. Deletion of key autophagy mediator Atg5 in embryonic fibroblasts (MEF cells) showed an autophagy dependent-NLRP3-inflammasome inhibition by antidepressant treatment. These results suggest the NLRP3-inflammasome could be a biomarker for antidepressant treatment response in MDD patients, and therefore the monitoring of NLRP3 expression levels and/or IL-1ß/IL-18 release may have clinical value in drug selection. Existing evidence suggests an anti-inflammatory effect of some antidepressants shown by IL-1ß, IL-6 and TNF-α. Our data have shown that antidepressant-mediated autophagy may have a role in restoration of certain metabolic and immunological pathways in MDD patients.